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PathoPhys GI > GI Mod 3 > Flashcards

GI Mod 3 Flashcards

1
Q

Pyloric Obstruction

A
  1. Narrowing of pylorus (junction between stomach and duodenum)
  2. Two forms…acquired or congenital
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2
Q

Infantile hypertrophic pyloric stenosis (IHPS) aka…Congenital pyloric stenosis

A 
Congenital” narrowing of pylorus
Signs/symptoms: 
•	infant at 2-3 weeks begins to vomit for no apparent reason
•	“projectile vomiting” – several feet
Frequency
•	infant disorder (3 per 1000 births)
•	Pathophysiology
•	Pyloric sphincter is hypertrophied
Etiology: 
•	not fully established 
•	hormones to allergic reactions have been suggested as potential causes
Treatment:
•	Surgery 
•	Pyloromyotomy:
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3
Q

Adult/Acquired Pyloric Obstruction

A
  • Usually caused by severe peptic ulcer or tumor in area
  • Vague s/s of epigatric discomfort/fullness with eating that progresses to severe epigastric discomfort
  • Gastric distention, nausea, progress to vomit and acute distress as obstruction develops over time
  • Treatment: address cause of obstruction
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4
Q

Adhesion- Mechanical Obstruction

A
  • Fibrous “scar tissue” adheres to intestinal loops

* Common complication of abdominal surgeries

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5
Q

Herniation- Mechanical Obstruction

A
  • Intestine protrudes through abdominal wall

* Intestine may strangulates through the opening…inguinal ring, umbilical hernia, hiatal hernia

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6
Q

Intussusception- Mechanical Obstruction

A
  • Telescoping of one part of an intestine on another portion

* More common in ileocecal area

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7
Q

Volvulus (Torsion)- Mechanical Obstruction

A
  • Intestine twist upon itself

* The mesentary “twists” around strangulating the blood supply to the intestine

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8
Q

Tumor Growth- Mechanical Obstruction

A

• Colon/rectal cancer is most common cause of large intestine obstruction

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9
Q

Paralytic Ileus Causes

A
  • Obstruction that results when peristalsis stops
  • Possible causes of ileus:
  • Use of certain drugs, such as narcotic pain drugs or high blood pressure medicine
  • Abdominal, spine or joint surgery
  • Injury or trauma
  • Infections/peritonitis
  • Heart attack
  • Imbalance of electrolytes
  • Disorders that affect muscle function
  • Low blood supply to parts of intestine (mesenteric ischemia
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10
Q

Treatment Strategies for Paralytic Ileus

A
  • NG tube to “decompress” pressure within GI tract
  • Address the underlying cause
  • If unsuccessful – surgery may be considered
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11
Q

Hirschsprung’s disease - congenital aganglionic megacolon

A

A. birth defect – ganglion (nerve) cells of the colon (large intestine ) fail to develop
1. 1 of every 5,000 newborns (M>F)
B. Functional result:
1. impaired motility of colon due to poor coordination/ability to contract intestinal musculature.
2. impacted/trapped stool, infection, inflammation, and constipation.

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12
Q

Categories/Types of Hirschprung’s Disease

A

Short-segment”
a. rectosigmoid colon

  1. “Long-segment”
    a. regions proximal to rectosigmoid are also involved
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13
Q

Treatment strategies for Hirschsprung’s disease

A
  1. decompress the colon (serial rectal irrigation) and surgical removal of involved intestinal segment
    a. Mild to moderate cases (e.g. short-segment disease)

b. Severe cases (e.g. enterocolitis)

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14
Q

Inflammatory Bowel Disease- IBD

A

A. Chronic autoimmune inflammatory disease that damages/ulcerates gastrointestinal tract

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15
Q

2 Types of IBD

A
  1. Crohn disease

2. Ulcerative colitis

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16
Q

Crohn’s Disease

A
  1. Crohn’s disease can affect any part of the GI tract, though it commonly occurs at the terminal end of the ileum of the SI and in the cecum of the LI.
  2. Stress may exacerbate symptoms but is not considered a cause of the disease
  3. Symptoms can range from mild to severe
17
Q

Epidemiology of Crohn’s

A

a. Estimated that 500,000 people in US have Crohn’s Disease (1-10 cases per 100,000)
b. Peak onset: 15-25 years (onset up to age 40)
c. Women more often affected than men
d. Familial history
e. 2-4x’s increased risk with first degree relative with disease

18
Q

Etiology of Crohn’s

A

a. Cause is poorly understood…the classic “general” theories…genetics, autoimmune and environmental factors.

19
Q

Pathophysiology of Crohn’s

A

a. Inflammation extends through all layers of intestinal wall
b. Chronic granulomatous inflammation
• Granuloma – cluster of cells that form in area of inflammation
c. May effects entire GI tract, mouth to anus
d. Distal ileum and proximal colon most often involved
e. Isolated colonic involvement in 25% of cases
f. “Skip lesions” – two or more inflamed areas with healthy bowel in-between

20
Q

Pharmaceutical Treatment for Crohn’s

A 
strategies depend on severity of symptoms 
a.	Anti-inflammatory drugs
•	Salicylate (5-ASA preparations)
•	Corticosteroids
•	Infliximab (Remicade)
b.	Immune suppressors
c.	Antibiotics
21
Q

Surgical Treatment for Crohn’s

A

a. Intestinal resection

b. Colostomy/ileostomy

22
Q

Ulcerative Colitis Pathophysiology

A
  1. Ulcerative colitis is chronic inflammatory disease that affects the large intestine.
  2. Pathophysiology
    a. Etiology unknown
    b. Inflammation “extends” to mucosa only (does not penetrate deeper layers)
    c. Always involves rectum and extends proximally to contiguous sections of colon
    d. May see different regional patterns of LI
    • Ulcerative proctitis
    • Proctosigmoiditis
    • Pancolitis
23
Q

Diverticulosis

A

Out-pockets” in intestinal wall

a. 85% of patients are asymptomatic
b. 15% develop colicky symptoms

24
Q

Pathophysiology of diverticulosis

A

a. Colonic muscle wall weak where vessels penetrate
b. Usually multiple diverticuli present (smaller size)
c. Distribution
• Most commonly found in sigmoid

25
Q

Treatment of Diverticulosis

A

a. High fiber diet
b. Avoid high residue foods (seeds, nuts, corn)
• Anecdotal strategy based on theory to prevent from small undigested peieces from getting lodge in diverticula – evidence not fully established

26
Q

Diverticulitis

A
  1. Inflammation of colonic diverticula
    a. Most often affects sigmoid colon
    b. Impacted with fecal material (fecalith)
    c. Colon perforations due to inflammation
    • Perforations may or may not penetrate intestinal wall
    • Simple diverticulitis

• Complicated diverticulitis

27
Q

Colorectal Cancer

A

A. estimated: 8.5% of all newly diagnosed of cancer in US
B. mortality related to CRC in U.S. > 500,000
C. Pathophysiology
1. Most CRC develop from adenomatous polyp
2. Initial mutant cancer cell develops in polyp
3. Slow growth on polyp as it progresses down the stalk toward the deeper layers of the mucosa
4. If cancer penetrates into sub-mucosal it can reaches lymphatic/BV pathways and become highly malignant
5. Screening for and removal of polyps critical for prevention

28
Q

Risk Factors for Colorectal Cancer

A
  1. Age >50 years
  2. Past Medical History
    a. IBD (Ulcerative Colitis)
    b. Adenomatous polyps >5mm
    c. Gall bladder surgery (cholecystectomy)
    d. Pelvic irradiation
  3. Family History
    a. First degree relative with colorectal cancer
    b. Familial adenomatous polyposis
    c. Hereditary non-polyposis colorectal cancer
  4. Lifestyle related risks
    a. Tobacco abuse
    b. Obesity (BMI > 35-40
29
Q

Screening for Colorectal Cancer

A
  1. Colonoscopy vs sigmoidoscopy
    a. Colonoscopy considered more thorough screening tool
    b. Flexible sigmoidoscopy limited in ability to screen
  2. Protocols
    a. Average risk patients > 50 yrs old
    • Colonoscopy every 10 yrs
    • Digital rectal exam and fecal occult blood yearly
    b. Patients with increased risk require more frequent or aggressive monitoring
30
Q

Hepatitis Pathophysiology

A 
A.	Viral hepatitis types A,B,C,D,E, & G 
B.	Pathology
1.	Hepatic cell death/scarring
2.	Kupffer cell hyperplasia
3.	Inflammation may disrupt canaliculi 
C.	Hepatic cell damage more severe in hepatitis B and C
D.	Fulminating hepatitis
1.	rare complication in which massive hepatic cell death and liver failure
31
Q

Cirrhosis

A

A. Irreversible inflammatory condition
B. Considered one of the leading causes of death in US
C. Many different disorders cause cirrhosis
D. Pathology (dependent on cause)
1. hepatic tissue becomes nodular and fibrotic
2. Size of liver may expand or shrink

32
Q

Alcoholic cirrhosis

A
  1. Initial phase
    a. Fatty accumulation develops within hepatocytes
  2. Chronic alcohol metabolism
    a. metabolism of alcohol produces acetaldehyde which disrupts hepatocyte function/metabolism
    b. cell damage initiates an inflammatory response and necrosis
    c. promotes excessive collagen synthesis and fibrotic accumulation/scarring
  3. Fibrosis eventually alter biliary and vascular drainage
    a. Multiple system effects
    • Liver function declines
    • Portal hypertension
    • GI bleeding, varicose veins, ascities
    • Heptomegaly, spleenomegaly
33
Q

Primary biliary cirrhosis

A

a. Autoimmune disease that attacks small intrahepatic bile ducts (canaliculi)
b. Inflammation of “duct system” leads to fibrotic changes

34
Q

Secondary biliary cirrhosis

A

a. Develops as result of chronic obstruction of biliary flow
b. Obstruction leads to inflammation which leads to fibrotic changes
c. Treatment: address the cause of obstruction

PathoPhys GI (4 decks)

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